Arq. Bras. Cardiol. 2018; 111(2): 191-192
Cardiac Sympathetic Activity and the Neuro-Humoral Theory on Heart Failure with Reduced Ejection Fraction: Have We Learned Enough?
DOI: 10.5935/abc.20180148
This Short Editorial is referred by the Research article "Sympathetic Dysautonomia in Heart Failure by 123I-MIBG: comparison between Chagasic, non-Chagasic and heart transplant patients".
Since the 1970s,, in observational trials, and more recently in placebo-controlled randomized trials,, antagonizing beta-1 adrenergic receptors in the myocardium has been shown to mitigate the burden of heart failure with reduced ejection fraction (HFrEF). Mortality has been reduced by 34-65% according to these studies. However, inhibiting the action of the peripheral sympathetic nervous system (SNS) by blocking alpha1 or stimulating alpha-2 central receptors has shown negative results or even an increased mortality, despite reducing norepinephrine plasma levels.– This indicates that SNS effects on myocardial receptors, more than in peripheral receptors, play a pivotal role in HFrEF pathophysiology.
Hyper-activation of the SNS and the renin-angiotensin-aldosterone axis, combined with an increase in load-dependent peptides and inflammatory cascades constitute the neuro-humoral theory on HFrEF progression. While the neuro-humoral response counteracts and compensates for an initial myocardial insult, in the long-term it contributes to the progression of the disease to the point that cardiovascular homeostasis eventually succumbs if not treated properly. Therapies targeting all these neuro-humoral responses have dramatically changed the natural history of HFrEF.
[…]
986